Iron is required for oxygen transport, oxidative phosphorylation, DNA synthesis, and other cellular processes. Iron co-factors, for example, iron-sulfur (Fe—S) clusters and heme, are synthesized by mitochondria and needed for mitochondrial function. Mitochondria supply energy for cells, including the energy needed by cardiomyocytes for repeated heart muscle contraction. Accordingly, the maintenance of mitochondria, including the removal of dysfunctional mitochondria through mitophagy and synthesis of iron co-factors, is needed for cardiomyocyte function.
Improper cardiomyocyte function may lead to heart failure. Heart failure may be further complicated by the presence of iron deficiency. Up to 50% of patients with heart failure have iron deficiency, which is associated with poor outcomes despite current therapies.
Accordingly, a need exists for the identification and development of new therapies for heart failure.